ArticleTranslational cancer research2022
Down-regulation of CX43 expression by miR-1 inhibits the proliferation and invasion of glioma cells.
Article in Translational cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Transcriptomic regulation of the hypothalamic-pituitary axis by GnRH immunization in Xizang sheep.Animal biotechnology · 2026Article
- Cx43 modulates malignant phenotypes in bladder cancer cells via the c-Src/PTEN/FAK axis.Journal of molecular histology · 2026Article
- Connexin 43 drives glioblastoma cancer stem cell phenotypes through a WNK lysine-deficient protein kinase 1-c-MYC signaling axis.Cell reports · 2025Article
- Bibliometric analysis and visualization of Connexin 43 in the field of solid tumor research(2000-2024).Frontiers in immunology · 2025Article
- Connexin-43 in Cancer: Above and Beyond Gap Junctions!Cancers · 2024Review
- Chlorpromazine overcomes temozolomide resistance in glioblastoma by inhibiting Cx43 and essential DNA repair pathways.Journal of translational medicine · 2024Article
- Deciphering Glioblastoma: Fundamental and Novel Insights into the Biology and Therapeutic Strategies of Gliomas.Current issues in molecular biology · 2024Review
- Connexin 43 in the function and homeostasis of osteocytes: a narrative review.Annals of joint · 2024Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Connexin (CX) 43 makes glioblastoma resistant to temozolomide, the first-line chemotherapy drug. However, targeting CX43 is very difficult because the mechanisms underlying CX43-mediated resistance remain unclear. CX43 is highly expressed in glioblastoma, which is closely associated with poor prognosis and chemotherapy resistance. The present study was to analyze the mechanism of microRNA (miR)-1 in regulating the proliferation and invasion of glioma cells. Methods: The effects of knockdown of miR-1 on the growth of glioma cell lines were observed by establishing blank, miR-1 inhibitor, and miR-1 mimic groups. Cell proliferation was detected using a Cell Counting Kit-8 (CCK-8) assay, cell apoptosis was detected by flow cytometry, and protein expression was detected by western blot. We used the Student's Results: Compared with the mimics normal control (NC) group, the apoptosis rate of the miR-1-3p mimics group was decreased, while that of the miR-1-3p inhibitor group was increased compared to the inhibitor NC group. In addition, the miR-1-3p mimics model of U251 cells exerted an inhibitory effect on the invasion ability of cells, whereas the miR-1-3p inhibitor model of U251 cells showed an invasion-promoting effect. The dual-luciferase assay showed that miR-1-3p had a targeted relationship with the CX43 gene. Conclusions: Down-regulation of CX43 expression by miR-1 inhibited the infiltration and growth of glioma cells and further promoted the apoptosis of glioma cells by regulating CX43 expression.
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